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October 19, 2016

How Insulin Resistance, Metabolic Disease Begin

Science is sometimes wrong and at other
times very revealing. The answer may not be simple, but a study published Sept. 26 in the Journal of Clinical Investigation adds to
growing research linking excessive sugar consumption, specifically
the sugar fructose, to a rise in metabolic disease worldwide.

The study, conducted in mice and
corroborated in human liver samples, unveils a metabolic process that
could upend previous ideas about how the body becomes resistant to
insulin and eventually develops diabetes.

"There is still significant
controversy as to whether sugar consumption is a major contributor to
the development of diabetes," said senior author Mark
Herman, M.D., assistant professor in the Division of Endocrinology,
Metabolism, and Nutrition at Duke University School of Medicine.

"Some investigators contend
that commonly consumed amounts of sugar do not contribute to this
epidemic," Herman said. "While others are convinced
that excessive sugar ingestion is a major cause. This paper reveals a
specific mechanism by which consuming fructose in large amounts, such
as in soda, can cause problems."

Insulin is a key hormone that regulates
blood glucose after eating. Insulin resistance, when the body's
metabolic tissues stop responding normally to insulin, is one of the
earliest detectable changes in the progression to diabetes.

However, according to this study, the
cause of insulin resistance may have little to do with defects in
insulin signaling and might actually be caused by a separate process
triggered by excess sugar in the liver that activates a molecular
factor known as carbohydrate-responsive element-binding protein, or
ChREBP.

The ChREBP protein is found in several
metabolic organs in mice, humans and other mammals. In the liver, it
is activated after eating fructose, a form of sugar naturally found
in fruits and vegetables, but also added to many processed foods
including soft drinks. The study found that fructose initiates a
process that causes the liver to keep making glucose and raising
blood glucose levels, even as insulin tries to keep glucose
production in check.

"For the past several decades,
investigators have suggested that there must be a problem in the way
the liver senses insulin, and that is why insulin-resistant people
make too much glucose," Herman said. "We found that
no matter how much insulin the pancreas made, it couldn't override
the processes started by this protein, ChREBP, to stimulate glucose
production. This would ultimately cause blood sugar and insulin
levels to increase, which over time can lead to insulin resistance
elsewhere in the body."

To test their hypothesis, researchers
studied mice that were genetically altered so their liver insulin
signaling pathways were maximally activated -- in other words, their
livers should not have been able to produce any glucose.

The researchers found that even in
these mice, eating fructose triggered ChREBP-related processes in the
liver, causing it to make more and more glucose, despite insulin
signals telling it to stop.

Previous studies have reported that
high fructose diets can cause multiple metabolic problems in humans
and animals, including insulin resistance and fatty liver disease.
Because most people found to be insulin-resistant also have fatty
liver, many investigators have proposed that the fructose-induced
fatty liver leads to liver dysfunction, which causes insulin
resistance, diabetes and high risk for heart disease.

The new findings suggest fatty liver
disease may be a red herring, Herman said. The likely cause of
insulin resistance may not be the buildup of fat in the liver, as
commonly believed, but rather the processes activated by ChREBP,
which may then contribute to the development of both fatty liver and
increased glucose production.

Although much more research is
required, the scientists believe they better understand a key
mechanism leading to pre-diabetes and can now explore how to possibly
interrupt that chain of events. ChREBP may not be the only pathway by
which this happens, and the protein may also be activated in other
ways, Herman said. But the study provides an important lead, he said.

"It gives us some insight into
what may be happening early in diabetes," Herman said.
"If we can develop drugs to target this process, this may be a
way to prevent the process early in the development of the disease."

The finding could also help scientists
one day diagnose metabolic disorders earlier on, potentially allowing
patients to make changes to their diets and lifestyles sooner to
prevent more serious complications.

As a medical doctor, Herman said the
advice to patients remains the same: make sure you're not eating too
much sugar, which often shows up on labels as sucrose (the main
ingredient in beet and cane sugar) and high fructose corn syrup.
Both sweeteners contain both glucose and fructose and are rapidly
absorbed, he said.

In its naturally occurring form and
quantity, fructose is not particularly harmful, Herman explained,
because if you're eating an apple, for example, you're eating a
relatively small amount of sugar and it's combined with other
nutrients such as fiber that may slow its absorption.

"You could eat three apples and
not get the same amount of fructose you might get from a 20-ounce
sugar-sweetened beverage," he said. "The major
sources of excessive fructose are in foods like sodas and many
processed foods, which are foods most doctors would say to limit in
your diet."

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About Me

I am enjoying life, despite diabetes type 2. I am retired and enjoying the time I have for writing and photography. I was diagnosed with type 2 on Oct 2003, on oral meds for 4 months and they were doing nothing to really improve my daily readings. By cutting my carbohydrates I received the most improvement, but still not enough. Then I requested insulin, even though I did not like the thought of needles. That brought about the biggest change and A1c's in the lower 6's and upper 5's. Now I am working at maintaining them under 6.0 and hopefully nearer 5.5.